ACUTE RENAL FAILURE OR ACUTE KIDNEY INJURY

Complications of Acute Renal Failure (ARF)

Potential complications of acute renal failure include:

 Fluid buildup: Acute renal failure may lead to a buildup in the lungs, which can cause shortness
of breath.
 Chest pain: If the lining that covers the heart (pericardium) becomes inflamed, they may
experience chest pain.
 Muscle weakness: When the body’s fluids and electrolytes- the body’s blood chemistry-are out of
balance, muscle weakness can result. Elevated levels of potassium in the blood are particularly
dangerous.
 Permanent kidney damage: Occasionally, acute kidney failure causes permanent loss of kidney
function, or end-stage renal disease. People with end-stage renal disease require permanent
dialysis- a mechanical filtration process used to remove toxins and waste from the body-or a
kidney transplant to survive.
 Death: Acute renal failure can lead to loss of kidney function and, ultimately, death. The risk of
death is higher in people with kidney problems before acute renal failure.
 Electrolyte disturbance:
 Hyperkalemia:(serum K+ >5.5mEq/L): decreased renal excretion combined with tissue
necrosis or hemolysis.
 Hyponatremia:(serum Na+<135mEq/L): excessive water intake in the face of excretory
failure.
 Hyperphosphatemia:(serum phosphate concentration of >5.5mg/dl): failure of excretion
or tissue necrosis.
 Hypocalcemia:(serum Ca2+ <8.5mg/dl): results from decreased Active Vit-D,
hyperphosphatemia, or hypoalbuminemia.
 Hypercalcemia:(serum Ca2+ > 10.5mg/dl): may occur during the recovery phase
following rhabdomyolysis included acute renal failure.
 Metabolic acidosis:(arterial blood ph <7.35): is associated with sepsis or severe heart
failure.
 Hyperuricemia: due to decreased uric acid excretion.
 Bleedind tendency: may occur due to platelet dysfunction and coagulopathy associated
with sepsis.
 Seizure: may occur related to uremia.

Classification of Acute Renal Failure (ARF)

Acute renal failure is classified under three categories:

 RIFLE criteria
 Acute Kidney Injury Network (AKIN)
 KDIGO Clinical Practice Guidelines

RIFLE criteria
Stage GFR Urine output
Risk ↑SCr×1.5 or ↓GRF >25% <0.5ml/kg/hr×6hour
Injury ↑SCr×2 or ↓GRF >50% <0.5ml/kg/hr×12hour
Failure ↑SCr×3 or ↓GFR >75% or <0.3ml/kg/hr×24hour or
baseline SCr ≥353.6µmol/L anuria×12hour
(≥4mg/dl) ↑SCr > 44.2µmol/L
(>0.5mg/dl)
Loss Complete loss of kidney function > 4 weeks
ESRD Complete loss of kidney function > 3 months

Acute Kidney Injury Network (AKIN) criteria:

 Abrupt (within 48h) reduction in kidney function currently defined as an absolute increase in
serum creatinine of 0.3mg/dl or more (≥26.4µmol/L) OR
 A percentage increase in serum creatinine of 50% or more (1.5 fold from baseline) OR
 A reduction in urine output (documented oliguria of <0.5ml/kg/hr for >6hr).

KDIGO Clinical Practice Guidelines:

 Increase in serum creatinine by 0.3mg/dl or more within 48 hours OR

 Increase in serum creatinine to 1.5 times baseline or more within the last 7days OR
 Urine output less than 0.5ml/kg/hr for 6 hours.

Drugs causing Acute Kidney Injury

Pre-renal Intrinsic Post-renal

Diuretics Radiocontrast dye Indinavir
ACE inhibitors Aminoglycosides Acyclovir
ARBs Foscarnet Sulfonamides
NSAIDs Amphotericin B
Cyclosporins Penicillins
Interferon Rifampin
Interleukin-2 Immunoglobulin
Tacrolimus Methotrexate
Lithium
Tetracyclines
Phenytoin
Cimetidine
Cocaine
Mannitol
Statins
Cidofovir
Pentamidine
Fluoroquinolones
Allopurinol
Cisplatin
Cephalosporins
Thiazide diuretics
 Ifosfamide
Indinavir
Gold
Mesalamine

Causes of Acute Renal Failure

Causes of pre-renal AKI

Reduced renal artery blood flow

 Volume losses
 Hemorrhage
 GI fluid losses: vomiting/diarrhea
 Burns
 Excessive diuresis
 Renal arterial obstruction
 Renal artery thrombosis/embolus
 Renal artery stenosis
 Aortic aneurysm
 Intra-renal ischemia
 Cardiogenic shock
 Sysytemic sepsis
 Hepatorenal failure
 Anaphylactic shock
 Nephrotic syndrome
 Abdominal compartment syndrome
 Page kidney
 Renal vein thrombosis
 Drugs
 COX-1 and -2 inhibitors
 ACEIs and ARBs
 Calcineurin inhibitors

Causes of intrinsic AKI:

Small vessel vascular disease

 Occlusion
 Cholesterol emboli
 Cryoglobulinemia
 HUS/TTP
 Disseminated Intravascular Coagulation (DIC)
 Plasmodium malaria
 Sickle cell crisis
  Eclampsia
 Vasculitis
 Microscopic polyangitis
 Wegener’s granulomatosis
 SLE
 Henoch-Schonlein Purpura
 Hyperacute renal transplant rejection
 Hypertension
 Malignant hypertension
 Scleroderma

Acute glomerulonephritis

 Crescentic rapidly progressive GN

 Anti-GBM disease
 Post infectious GN
 Idiopathic

Interstitial nephritis

 Drug-associated
 Antibiotics
 NSAIDs
 Post-infection
 Leptospirosis
 Epstein-Barr virus
 Drug-toxicity
 Aminoglycosides
 Tenovir
 Toxins
 Radiocontrast media
 Myoglobin
 Hemolysis
 Myeloma/light chains
 Snake/spider venom
 Heavy metals
 Cisplatin
 Poisons
 Plant
 Drugs
 Chemicals (e.g., ethylene glycol)
 Crystals
 Urate
 Indinavir
 Oxalate
  Infiltartion
 Sarcoid
 Lymphoma

Infection

 Acute pyelonephritis
 Bacterial infection

Immunological

 Renal transplantation
 Cellular rejection

Causes of post-renal (obstructive) AKI:

Intrinsic

 Intraluminal
 Calculus
 Blood clot
 Sloughed papilla
 Intramural
 Ureteric malignancy
 Ureteric stricture (TB)
 Post-irradiation fibrosis
 Bladder cancer
 Prostatic hypertrophy

Extrinsic

 Extramural
 Retroperitoneal fibrosis
 Pelvic malignancy
 Ureteric ligation

Definition of Acute Renal Failure

Abrupt (1-7days) and sustained (>24h) decrease in GFR (Glomerular Filtration Rate), urine output or
both.

Management of acute renal failure

Prevention

 Because there are no specific therapies for ischemia or nephrotoxic AKI,

 Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and
intravascular volume in high-risk patients, such as the elderly and those with pre-existing renal
insufficiency.
 Indeed, aggressive retoration of intravascular volume has deen shown to reduce the incidence of
ischemic AKI dramatically after major surgery or trauma, burns, or cholera prevention is of
paramount importance
 The incidence of nephrotoxic ARF can be reduced by tailoring the dosage of potential
nephrotoxinsto body size and GFR, for example, reducing the dose or frequency od
administration of drugs in patients with pre-exsiting renal impairment
 Preliminary measures:
 Exclusion of reversible causes: Obstruction should be relived, infection should be treated
 Correction of pre-renal factors: intravascular volume and cardiac performance should be
optimised
 Maintenance of urine output: Loop diuretics may be usefully to convert the oliguric form of ATN
to the non-oliguric form
 High doses of loop diuretics such as Furosemide (upto 200 to 400mg intravenously) may promote
diuresis in patients who fail to respond to conventional doses
 Specific therapies:
 To date, there are no specific therapies for established intrinsic renal ARF due to
ischemia or nephrotoxicity
 Management of these disorders should focus on elimination of the causative
hemodynamic abnormality or toxin, avoidance of additional insults, and prevention and
treatment of complications.
 Specific treatment of other causes of intrinsic renal ARF depends on the underlying
pathology.

Pre-renal ARF

 The composition of replacement fluids for treatment of pre-renal ARF due to hypovolemia must
be tailored according to the composition of the lost fluid.
 Severe hypovolemia due to hemorrhage should be corrected with packed red blood cells ,
whereas isotonic saline is usually appropriate replacement for mild to moderate hemorhage or
plasma loss (e.g., burns, pancreatitis).
 Urinary and gastrointestinal fluids can vary greatly in composition but are usually hypotonic
solutions (e.g., 0.45% saline) are usually recommended as initial replacement in patients with pre-
renal ARF due to increased urinay or gastrointestinal fluid losses, although isotonic saline may be
more appropriate in severe cases.
 Subsequent therapy should be based on measurements of the volume and ionic content of
excreted or drained fluids. Serum potassium and acid-base status should be monitored carefully.

Post-renal ARF

 Management of post-renal ARF requires closed collaboration between nephrologist, urologist,

and radiologist.
  Obstruction of the urethra or bladder neck is usually managed initially by transurethral or
suprapubic placement of a bladder catheter, which provides temporary relief while the obstructing
lesion, is identified nad treated definitively. Similarly, ureteric obstruction may be treated initially
by percutaneous catherterization of the dilated renal pelvis or ureter.

Supportive Measures (Conservative therapy)

 Dietary management
 Generally, sufficient calorie reflects a diet that provide 40-60gms of protein and and 35-
50kcal/kg lean body weight
 In some patients, severe catabolism occurs and protein supplementation to achieve
1.25gm of protein/kg body weight is required to mainatin nitrogen balance
 Restricting dietary protein to approximately 0.6g/kg/day of protein of high biological
value (i.e., rich in essential amino acids) may be recommended in severe azotemia.
 Fluid and electrolyte management
 Following correction of hypovolemia, total or and intravenous fluid administration
should be equal to daily sensible losses (via urine, stool, and NG tune surgical drainage)
plus estimated insensible (i.e., respiratory and derma) losses which manually equals 400-
500ml/day. Strict input output monitoring is important.
 Hypervolemia: can usually be managed by restriction of salt and water intake and
diuresis
 Metabolic acidosis: is not treated unless serum bicarbonate concentartion falls below
15mmol/L or arterial ph falls below 7.2
 More severe acidosis is corrected by oral or intravenous sodium bicarbonate
 Initial rates of replacement are guided by estimates of bicarbonate deficit and adjusted
thereafter according to serum levels.
 Patients are monitored for complications of bicarbonate administration such as
hypervolemia, metabolic acidosis, hypocalcemia, and hypokalemia.
 From a practical point of view, most patients requiring sodium bicarbonate need
emergency dialysis within days.
Hyperkalemia: cardiac and neurologic complications may occur if serum K+ level is
>6.5mEq/L
 Restrict dietary K+ intake
 Give calcium gluconate 10ml of 10% solution over 5mins
 Glucose solution 50ml of 50% glucose plus Insulin 10 units IV
 Give potassium-binding ion exchange resins
 Dialysis: if medical therapy fails or the the patient is very toxic
 Hyperphosphatemia is usually controlled by restriction of dietary phosphate and by oral
aluminium hydroxide or calcium carbonate, which reduce gastrointestinal absorption of
phosphate.
 Hypocalcemia doesnot usually require treatment.
 Anemia: may necessiate blood transfusion if severe or if recovery is delayed.
 GI bleeding: Regular dose of antacids appear to reduce the incidence of gastrointestinal
hemorrhage significantly and may be more effective in this regard than H2 antagonists, or proton
pump inhibitors
 Meticulous care of intravenous cannulae, baldder catheters, and other invasive devices is
mandatory to avoid infections.

Dialysis

 Indications and Modalities of Dialysis:

Dialysis replaces renal function until regeneration and repair restore renal function.
Hemodialysis and peritoneal dialysis appear equally effective for management of ARF.
 Absoulte indications for dialysis include:
 Symptoms or signs of the uremic symdrome
 Refractory hypervolemia
 Severe hyperkalemia
 Metabolic acidosis.